Abcg1, an ATP-binding cassette half transporter, is crucial for facilitating the efflux of excess cholesterol from macrophages and other cells [2]. It is part of the reverse cholesterol transport (RCT) pathway, where it contributes to the continued cholesterol efflux to high-density lipoprotein (HDL) for its maturation, thus maintaining cellular cholesterol homeostasis [1]. This function is vital as excessive cholesterol accumulation in cells is toxic and is a key factor in diseases like atherosclerotic cardiovascular disease [1]. Genetic models, such as KO or CKO mouse models, can provide in-depth insights into its function.

In myeloid-lineage Abcg1-deficient mice, there was an ameliorated inflammatory status in adipose tissue and reduced insulin resistance. Abcg1-deficient adipose tissue macrophages (ATMs) showed a less inflammatory phenotype, modified fatty acid (FA) metabolism, and a shift in FA pools, redirecting saturated FAs from membrane phospholipids to lipid droplets [3]. These findings from the mouse model demonstrate that Abcg1 plays a role in orchestrating ATM plasticity and insulin resistance in diet-induced obesity (DIO) by rewiring saturated FA pools [3].

In conclusion, Abcg1 is essential for maintaining cellular cholesterol homeostasis through its role in cholesterol efflux. The use of Abcg1-deficient mouse models has revealed its significance in adipose tissue inflammation and insulin resistance, providing valuable insights into its function in metabolic diseases such as DIO [3].